Cannabinoid agonists have been shown to lower intra-ocular pressure in glaucoma; produce pain relief; lessen nausea associated with chemotherapy; produce a neuroprotective effect in neurodegenerative diseases such as Alzheimer's disease and amyotrophic lateral sclerosis (ALS); and act as appetite stimulants. Commercial development of ligands that bind to the cannabinoid CB1 receptor have hit major roadblocks due to psychoactive effects associated with agonists and depressive effects, including suicidal ideation, associated with inverse agonists. Until very recently, the focus of cannabinoid compound design was on the G-protein signaling pathway. It has now become clear that there are two signaling pathways for the CB1 receptor, the long-appreciated Gi/o pathway (which leads to a pERK signal that can be abrogated with pertussis toxin, a Gi/o toxin) and a beta-arrestin mediated pathway that leads to production of pERK that is insensitive to pertussis toxin. Ligands that favor such a second pathway have been discovered in other receptor fields (the beta-2-adrenergic and delta-opioid fields), but these latter ligands actually signal through both pathways, simply favoring the beta-arrestin mediated pathway. What is needed are tools for determining which effects of CB1 modulators arise from which pathways and therapeutically effective cannabinoid CB1 receptor ligands having reduced adverse side effects. The present invention meets these and other needs.